TY - JOUR
T1 - Interaction between parathyroid hormone and endogenous estrogen in normal women
AU - Buchanan, James R.
AU - Santen, Richard J.
AU - Cavaliere, Anthony
AU - Cauffman, Susanne W.
AU - Greer, Robert B.
AU - Demers, Laurence M.
N1 - Funding Information:
From the Division of Orthopaedic Surgery and the Division of Endocrinology, Department of Pathology, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pa. Supported by the Merck Corporation and Laverty Foundation. Address reprint requests to James R. Buchanan, MD, Division of Orthopaedic Surgery, Milton S. Hershey Medical Center, Pennsylvania State University. Hershey, PA 17033. o I986 by Grune & Stratton, Inc. 0026-0495/86/3506-0003$03.00/0
PY - 1986/6
Y1 - 1986/6
N2 - It has been hypothesized that estrogens conserve bone substance by blocking the resorbing effect of parathyroid hormone (PTH). We evaluated this hypothesis by examining the relation of circulating PTH to endogenous estrogen fluctuation during four quarters of a single menstrual cycle in 20 normal women. The hypothesis predicts that PTH should vary directly with estrogen, since PTH should increase following estrogen elevation to satisfy physiologic demands for calcium. Contrary to the predicted direct variation, PTH remained constant throughout the menstrual cycle despite sharply fluctuating estrogen levels. Furthermore, PTH was negatively associated with estrone during the early follicular (r = -.65, P < 0.005) and late follicular (r = -.84, P < 0.0001) phases. We attempted to determine whether this unexpected relationship between estrone and PTH signified a direct physiologic link, by excluding factors which could have spuriously engendered the inverse correlation. Stepwise multiple regression and partial correlation showed that estrone contributed significantly to circulating PTH independent of the effects of dietary calcium, 25-hydroxyvitamin D, serum calcium, 1,25-dihydroxyvitamin D, phosphate, estradiol, progesterone, and body weight. Therefore, it is possible that the inverse correlation between estrone and PTH signified a direct physiologic link, as an artifactual cause for the relationship could not be identified. These data imply that estrone interacts with PTH, but not by blocking PTH-mediated bone resorption. We conclude that estrone is associated with reduced circulating PTH through an as yet undetermined mechanism.
AB - It has been hypothesized that estrogens conserve bone substance by blocking the resorbing effect of parathyroid hormone (PTH). We evaluated this hypothesis by examining the relation of circulating PTH to endogenous estrogen fluctuation during four quarters of a single menstrual cycle in 20 normal women. The hypothesis predicts that PTH should vary directly with estrogen, since PTH should increase following estrogen elevation to satisfy physiologic demands for calcium. Contrary to the predicted direct variation, PTH remained constant throughout the menstrual cycle despite sharply fluctuating estrogen levels. Furthermore, PTH was negatively associated with estrone during the early follicular (r = -.65, P < 0.005) and late follicular (r = -.84, P < 0.0001) phases. We attempted to determine whether this unexpected relationship between estrone and PTH signified a direct physiologic link, by excluding factors which could have spuriously engendered the inverse correlation. Stepwise multiple regression and partial correlation showed that estrone contributed significantly to circulating PTH independent of the effects of dietary calcium, 25-hydroxyvitamin D, serum calcium, 1,25-dihydroxyvitamin D, phosphate, estradiol, progesterone, and body weight. Therefore, it is possible that the inverse correlation between estrone and PTH signified a direct physiologic link, as an artifactual cause for the relationship could not be identified. These data imply that estrone interacts with PTH, but not by blocking PTH-mediated bone resorption. We conclude that estrone is associated with reduced circulating PTH through an as yet undetermined mechanism.
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U2 - 10.1016/0026-0495(86)90003-X
DO - 10.1016/0026-0495(86)90003-X
M3 - Article
C2 - 3754923
AN - SCOPUS:0022569759
SN - 0026-0495
VL - 35
SP - 489
EP - 494
JO - Metabolism
JF - Metabolism
IS - 6
ER -